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Identification of ten loci associated with height highlights new biological pathways in human growth
 

Summary: Identification of ten loci associated with height highlights
new biological pathways in human growth
Guillaume Lettre1,2, Anne U Jackson3,25, Christian Gieger4,5,25, Fredrick R Schumacher6,7,25, Sonja I Berndt8,25,
Serena Sanna3,9,25, Susana Eyheramendy4,5, Benjamin F Voight1,10, Johannah L Butler2, Candace Guiducci1,
Thomas Illig4, Rachel Hackett1, Iris M Heid4,5, Kevin B Jacobs11, Valeriya Lyssenko12, Manuela Uda9,
The Diabetes Genetics Initiative24, FUSION24, KORA24, The Prostate, Lung Colorectal and Ovarian Cancer
Screening Trial24, The Nurses' Health Study24, SardiNIA24, Michael Boehnke3, Stephen J Chanock13,
Leif C Groop12,14, Frank B Hu6,7,15, Bo Isomaa16,17, Peter Kraft7, Leena Peltonen1,18,19, Veikko Salomaa20,
David Schlessinger21, David J Hunter1,6,7,15, Richard B Hayes8, GoncŞalo R Abecasis3, H-Erich Wichmann4,5,
Karen L Mohlke22 & Joel N Hirschhorn1,2,23
Height is a classic polygenic trait, reflecting the combined influence of multiple as-yet-undiscovered genetic factors. We carried
out a meta-analysis of genome-wide association study data of height from 15,821 individuals at 2.2 million SNPs, and followed up
the strongest findings in 410,000 subjects. Ten newly identified and two previously reported loci were strongly associated with
variation in height (P values from 4 ┬ 10└7 to 8 ┬ 10└22). Together, these 12 loci account for B2% of the population variation
in height. Individuals with r8 height-increasing alleles and Z16 height-increasing alleles differ in height by B3.5 cm. The newly
identified loci, along with several additional loci with strongly suggestive associations, encompass both strong biological
candidates and unexpected genes, and highlight several pathways (let-7 targets, chromatin remodeling proteins and Hedgehog
signaling) as important regulators of human stature. These results expand the picture of the biological regulation of human height
and of the genetic architecture of this classical complex trait.
The advent of genome-wide association studies1, made possible

  

Source: Abecasis, Goncalo - Department of Biostatistics, University of Michigan

 

Collections: Biology and Medicine; Mathematics